Physiology of Feeding and Satiety Flashcards

(40 cards)

1
Q

what is energy homeostasis

A

Physiological process whereby energy intake is matched to energy expenditure over time

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2
Q

what is obesity

A

metabolic syndrome characterised by central obesity, dyslipidemia, insulin resistance= type 2 diabetes, cardiovascular disease

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3
Q

how is obesity viewed

A

as a disease and a disability

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4
Q

what are the major factors influencing obesity

A

genetics; susceptibility genes

environment

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5
Q

what diseases are associated with obesity

A

type 2 diabetes, hypertension, heart attack, certain cancers, osteoarthritis, heart disease, resp disease (sleep apnea), stroke, dementia, fatty liver

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6
Q

why do we need fat

A

energy storage, prevention of starvation, energy buffer during prolonged illness

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7
Q

why does the brain make it difficult to lose weight

A

increased body fat alters brain function, induces re-programming where it view the extra weight as normal and dieting as a threat to survival

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8
Q

how does the CNS influence energy balance and body weight

A

behaviour (feeding and physical activity)
ANS (regulates energy expenditure)
neuroendocrine system (secretion of hormones)

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9
Q

what part of the brain is responsible for fat storage

A

hypothalamus

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10
Q

what three basic concepts underlie the control of energy intake and body weight

A

satiety signalling, adiposity negative feedback signalling,

food reward

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11
Q

what is satiation

A

sensation of fullness generated during a meal

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12
Q

what is satiety

A

period of time between termination of one meal and the initiation of the next

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13
Q

what is adiposity

A

the state of being obese

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14
Q

when do satiation signals increase

A

during meals to limit meal size

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15
Q

what are the satiation signals

A

cholecystokinin (CCK), peptide YY (PYY3-36), Glucagon-like peptide (GLP-1), oxyntomodulin (OXM), obestatin

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16
Q

what does cholecystokinin do and what secretes it

A

secreted from enteroendocrine cells
in duodenum and jejunum. Released in proportion to lipids and
proteins in meal. Signals via sensory nerves to hindbrain and
stimulates hindbrain directly (nucleus of solitary tract (NTS)).

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17
Q

what does peptide YY do and what secretes them

A

secreted from endocrine mucosal L-
cells of G-I tract. Levels increase rapidly post-prandially. Inhibits
gastric motility, slows emptying and reduces food intake (Hypo).

18
Q

what does glucagon like peptide 1 do

A

product of pro-glucagon
gene. Also released from L cells in response to food ingestion.
Inhibits gastric emptying and reduces food intake (Hypo, NTS)

19
Q

what does oxyntomodulin do and what secretes it

A

Also from pro-glucagon gene and
released from oxyntic cells of small intestine after meal. Acts
to suppress appetite – mechanism unclear.

20
Q

what does obestatin do and what secretes it

A

peptide produced from gene that encodes ghrelin
and released from cells lining stomach/small intestine.
Suggested to reduce food intake – may act to antagonise the
actions of ghrelin – actions unclear at present.

21
Q

what is ghrelin- what secretes it and what does it do

A

a hunger signal- Octanoylated peptide, produced and secreted by
oxyntic cells in stomach. Ghrelin levels increase before meals
and decrease after meals. Levels are raised by fasting and
hypoglycaemia.

Peripheral ghrelin stimulates food intake (Hypo) and decreases
fat utilization

22
Q

what central appetite controllers work to increase food uptake

A

Glutamate, Gaba and opioids increase food intake when
injected into hypothalamic centres - effects modest/short
lasting

23
Q

what central appetite controllers work to suppress food uptake

A

Monoamines act to suppress food intake - many drugs
developed to act on these systems - most withdrawn due
to side-effects.

24
Q

what are adiposity signals

A

hormones produced in peripheral tissues that act on hypothalamic neurons to tell the brain the status of body fat stores

25
what are the two adiposity hormones
leptin (made and released from fat cells) insulin (made and released from pancreatic cells)
26
how do hormones affect fat storage
``` Inform brain (hypothalamus) to alter energy balance - eat less and increase energy burn ``` This malfunctions in obese state
27
what is a spontaneous mutations that can cause obesity
Ob gene- produced leptin- when mutation reduced production mimicking starving, unrestrained appetite
28
a defect in what receptor can also cause obesity
leptin receptor
29
describe leptin
circulates in proportion to body adiposity high levels of leptin receptors (Ob-Rb) in hypothalamus intracerebroventricular (icv) leptin inhibits food intake and decreases body weight of rodents
30
what are the biological roles of peptin
Food intake/energy expenditure/fat deposition Peripheral glucose homeostasis/insulin sensitivity Maintenance of immune system Maintenance of reproductive system Angiogenesis Tumourigenesis Bone formation
31
describe insulin
circulates in proportion to body adiposity high levels of insulin receptors in hypothalamus intracerebroventricular (icv) insulin inhibits food intake and decreases body weight of rodents
32
what is food reward
pleasure derived from eating- dopamine pathways
33
how are 'ob' humans treated
48 months of leptin sc injections
34
what limits the use of leptin therapy in common obesity
leptin resistance
35
what are the two theroies behind leptin resistance
Defective leptin transport into brain Altered signal transduction following leptin binding to its receptor
36
what is a prescribed anti obesity drug and its side effects
rimonabant severe depression, anxiety and increased risk of suicide, to promote development of neurodegenerative disease,
37
what is an over the counter drug for obesity and how does it work
orlistat Inhibits pancreatic lipase decreasing triglyceride absorption Reduces efficiency of fat absorption (~30%) in small intestine Side-effects include cramping and severe diarrhoea Need to take vitamin supplements (fat soluble vitamins)
38
what is BAT
brown adipose tissue
39
what is adaptive thermogenesis
BAT dissipates energy as heat (thermogenic adipocytes) thermogensis is the increase energy expenditure uncoupling of oxidative metabolism from ATP production
40
what is a drug that can cause adative thermogenesis
2,4- dinitrophenol (DNP)